@article{mbs:/content/journal/jgv/10.1099/vir.0.19109-0, author = "Tuthill, Tobias J. and Papadopoulos, Nikolaos G. and Jourdan, Patrick and Challinor, Lisa J. and Sharp, Nigel A. and Plumpton, Chris and Shah, Ketaki and Barnard, Suzanne and Dash, Laura and Burnet, Jerome and Killington, Richard A. and Rowlands, David J. and Clarke, Neil J. and Blair, Edward D. and Johnston, Sebastian L.", title = "Mouse respiratory epithelial cells support efficient replication of human rhinovirus", journal= "Journal of General Virology", year = "2003", volume = "84", number = "10", pages = "2829-2836", doi = "https://doi.org/10.1099/vir.0.19109-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.19109-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Human rhinoviruses (HRV) are responsible for the majority of virus infections of the upper respiratory tract. Furthermore, HRV infection is associated with acute exacerbation of asthma and other chronic respiratory diseases of the lower respiratory tract. A small animal model of HRV-induced disease is required for the development of new therapies. However, existing mouse models of HRV infection are difficult to work with and until recently mouse cell lines were thought to be generally non-permissive for HRV replication in vitro. In this report we demonstrate that a virus of the minor receptor group, HRV1B, can infect and replicate in a mouse respiratory epithelial cell line (LA-4) more efficiently than in a mouse fibroblast cell line (L). The major receptor group virus HRV16 requires human intercellular adhesion molecule-1 (ICAM-1) for cell entry and therefore cannot infect LA-4 cells. However, transfection of in vitro-transcribed HRV16 RNA resulted in the replication of viral RNA and production of infectious virus. Expression of a chimeric ICAM-1 molecule, comprising mouse ICAM-1 with extracellular domains 1 and 2 replaced by the equivalent human domains, rendered the otherwise non-permissive mouse respiratory epithelial cell line susceptible to entry and efficient replication of HRV16. These observations suggest that the development of mouse models of respiratory tract infection by major as well as minor group HRV should be pursued.", }